Fig. 6

Inhibition of miR-96-5p reversed IL-1β-induced inflammatory factors and ECM changes in HNPCs by regulating the level of PPARγ. HNPCs were treated with IL-1β and /or transfected with miR-96-5p inhibitor and/or short hairpin PPARγ (groups: NC, IL-1β, IL-1β + miR-96-5p inhibitor, IL-1β + siPPARγ, IL-1β + miR-96-5p inhibitor + siPPARγ). A The mRNA level of PPARγ was determined by qRT-PCR. B, C The protein expression of PPARγ in HNPCs of each group was detected by Western blot. D The concentration of IL-6 in culture medium was detected by ELISA assay. E, F The protein expression of Col II, aggrecan, MMP3, MMP13, ADAMTS-4, and ADAMTS-5 related to ECM were detected by Western blot. (*P < 0.05, **P < 0.01, ***P < 0.001 vs. NC group; ^#P < 0.05, ^##P < 0.01 vs. IL-1β group; ^{^}P < 0.05, ^{^^}P < 0.01 vs. IL-1β + miR-96-5p inhibitor; ^&P < 0.05, ^&&P < 0.01 vs. IL-1β + siPPARγ). PPARγ, peroxisome proliferator-activated receptor γ; mRNA, messenger RNA; IL, interleukin; NC, normal control; siPPARγ, small interfering PPARγ; Col II, type II collagen; MMP, matrix metalloproteinase; ADAMT, A disintegrin and metalloproteinase with thrombospondin motifs; ECM, extracellular matrix; HNPCs, human nucleus pulposus cells; qRT-PCR, quantification real-time reverse transcription-polymerase chain reaction; ELISA, enzyme-linked immunosorbent assay